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layer before they can stimulate or inhibit receptor cells <br />(Getchell 1986). Increased mucification induced by contaminant <br />exposure increases thickness of the mucus coat (Sorensen 1991), <br />consequently time required for inhibitory solutes to diffuse to <br />olfactory receptors may increase. Miller and Mackay (1982) <br />showed that mucus is a strong copper chelater. Thus, in addition <br />to the physical advantages of a thicker mucus coat, the affinity <br />of mucus for contaminants may prevent diffusion to olfactory <br />receptors, and sloughing of excess mucus may physically remove <br />chelated toxicants from the olfactory chamber. Whitear (1992) <br />hypothesized that chemoreceptors in fish may have a <br />neuroendocrine link to surrounding cells in the epidermis. If <br />this function exists for olfactory receptors of fish, it may <br />influence mucus secretion of the epidermis by controlling goblet <br />and superficial epithelial cells. Such an association would <br />provide a basis for a feedback mechanism in which olfactory <br />receptor cells could optimize local mucus production by <br />increasing it when harmful solutes are present, and decreasing it <br />under normal conditions to improve sensitivity to <br />information-containing odorants. <br />A second explanation for the decrease in toxic effects at a <br />96-h exposure duration is that detoxifying mechanisms in <br />olfactory tissues may have become induced. The olfactory <br />epithelium of a number of fishes contains high levels of <br />cytochrome P-450 monooxygenase which can be activated by exposure <br />to heavy metals (Klaprat et al. 1992). Although the specificity <br />17 <br />